The early-onset periodontal diseases (EOP), including clinical syndromes designated localized juvenile periodontitis (LJP), generalized juvenile periodontitis (GJP), and rapidly progressive periodontitis (RPP), are characterized by their age of onset, which is usually after puberty, and the unusually rapid progression of periodontal attachment loss in affected individuals. EOP is also sometime manifested before puberty, and it is then called pre-pubertal periodontitis (PPP). The localized (LJP) and generalized (GJP, RPP) forms of EOP aid are distinguished by the pattern of teeth affected by such attachment loss. Classically, LJP has been defined by attachment loss at first molar and incisor teeth, while GJP affects a large number of teeth not limited to first molars and incisors.
EOP occurs after puberty but before age 35 and often results in pronounced tooth loss before the age of 20 years. The most recent National Survey of the Oral Health of U.S. Children aged 5 to 17 conducted in 1986-86 included periodontal assessment of 11,007 adolescents aged 14 to 17 years old. Nationwide, approximately 0.53% of these adolescents were estimated to have LJP, 0.13% had G-EOP, and 1.61% had incidental loss of attachment. If one projected these frequencies to the total U.S. population, one would estimate that approximately 70,000 persons aged 14 to 17 years old had LJP at the time of the survey and an additional 17,000 members of this age group has the more destructive G-EOP. Since both of these forms of EOP can also develop well after age 17 (by definition, up to age 35) the total number of EOP cases in the U.S. may be 2- to 4-fold higher than these numbers that are limited to the four year age range of the adolescent group. This means that from approximately 175,000 up to 350,000 EOP cases may exist in the U.S. population among the total adolescent and young adult population (age 14-35).
Recent studies have underscored the association of periodontal infections with certain medically important conditions. There are increasing data accumulating that implicate periodontal disease as a risk factor for cardiovascular diseases such as heart attack and stroke. See e.g. J. Beck et al., "Periodontal Disease and Cardiovascular Disease," J. Periodontol. 67:1123 (1996). Epidemiologic studies indicate that, even after accounting for other known risk factors for cardiovascular disease, the relative risk attributable to periodontal infections is significant. Secondly, recent studies have shown that mothers with periodontitis are at greater risk for having low weight babies than those without periodontitis. See Offenbacher et al., "Periodontal Infection as a Possible Risk Factor for Preterm Low Birth Weight," J. Periodontol. 67:1103 (1996).
Once symptoms are detected, treatment is difficult and expensive. It is believed that treatment results would be much better if individuals could be determined to be at risk prior to symptoms. In this manner, preventative measures could be taken and early intervention strategies could be employed. Unfortunately, determining concrete risk factors has been problematic.
Bacteria are recognized as the primary etiologic agents in periodontitis. Moreover, it is generally agreed that Actinobacillus actinomycetemcomitans is involved in the disease. However, microbial virulence appears to differ from person to person. Consequently, to date, no direct cause and effect relationship exists between any specific bacteria and type of periodontitis. As a result, the presence of a specific bacteria is not pathognomonic for any form of periodontitis. See T. A. Hart, "Genetic Risk Factors for Early-Onset Periodontitis," J Periodontol. 67:355 (1996).
Several putative genetic risk factors have been suggested for EOP, most of which are based upon data implicating aberrant host immunity or inflammatory reactions as likely pathogenic mechanisms. These factors include HLA antigens, factors related to aberrant polymorphonuclear leukocyte chemotactic function, and elevated or depressed cytokine and prostanoid production. See generally, H. A. Schenkein, "Genetics of Early-Onset Periodontal Diseases," In: Molecular Pathogenesis of Periodontal Disease (1994 ASM, Robert Genco, Ed.).
In all of the above-mentioned cases, it is hypothesized that the host response to bacterial etiologic agents is aberrant or deficient, resulting in expression of periodontitis at a young age. This hypothesis is supported by the observation that a number of defined genetic abnormalities associated with depressed phagocytic function predispose patients to periodontitis during early childhood. However, none of these risk factor studies have been consistently replicated, and most are based on small sample sizes and provide only weak statistical support for associations.
The actual genetic architecture of EOP susceptibility remains undetermined to date. What is needed is a reliable diagnostic based on genetic factors which identifies individuals at risk for EOP prior to the onset of symptoms. This would permit early monitoring and therapeutic intervention.